These findings, in conjunction with those in an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis) and others on amyotrophic lateral sclerosis (with some similar features and symptoms) wherein Nurr1 activation reduced severity of disease, provide functional relevance of our findings in human disease.15,16 Could enhancing Nurr1 expression in early multiple sclerosis and throughout the disease course limit cytotoxic T-cell inflammation and neuronal loss that contribute to multiple sclerosis progression? This evidence concerns the gene NR4A2 and experimental autoimmune encephalomyelitis.